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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 20 (1981), S. 399-405 
    ISSN: 1432-1041
    Keywords: alpha-adrenergic blocker ; hypertension ; blood pressure ; pulse rate ; noradrenaline ; plasma renin activity ; plasma aldosterone ; dopamine-beta-hydroxylase ; E-643
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary To determine whether E-643, a new α-blocking agent, would reduce the blood pressure, regardless of the posture, a 1 mg dose was given 3 times daily for 7 consecutive days, to 8 male and 7 female inpatients, aged 37–73 years, with essential hypertension. Blood pressure and pulse rate were measured daily in the supine, sitting and standing positions. Before and after the treatment with E-643, plasma levels of noradrenaline, adrenaline, dopamine-β-hydroxylase, renin and aldosterone were determined, samples being obtained with the subjects recumbent and after standing upright for 60 min. A significant reduction in the systolic and diastolic blood pressures was evident in the supine (172±31/100±12 → 151±28/89±14 mmHg), sitting (158±22/101±11 → 138±28/89±15 mmHg) and standing (153±32/103±21 → 129±31/89±20 mmHg) positions. The reduction in blood pressure remained unchanged throughout the period of administration of E-643. Pulse rate was not affected when the subjects were supine (67±10 → 69±10 beats/min), but was increased in the sitting (68±10 → 73±9 beats/min) and standing (73±10 → 81±11 beats/min) positions. The increased pulse rate tended to decline during continued administration of E-643. Treatment with E-643 produced no significant change in plasma levels of adrenaline, noradrenaline, dopamine-β-hydroxylase, renin and aldosterone. The antihypertensive effect of treatment was more prominent in the patients with higher levels of plasma catecholamines and dopamine-β-hydroxylase, and was less prominent in those with higher plasma renin and aldosterone. Two patients had temporary bouts of dizziness and visual disturbances, but there were no subjective complaints during treatment.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1041
    Keywords: Calcium channel blocker ; Nilvadipine ; blood pressure ; liver disease ; pharmacokinetics ; pharmacodynamics ; cirrhosis ; hepatitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Fourteen normotensive patients with liver disease (6 with cirrhosis and 8 with chronic hepatitis) and 7 healthy volunteers were given a single oral dose of nilvadipine 2 mg. In addition, nilvadipine 4 mg was administered orally twice daily for several months to 6 hypertensive patients with mild liver dysfunction and 18 hypertensives with normal liver function. A significant increase in plasma nilvadipine was found in the patients with cirrhosis as compared both to the normal and chronic hepatitis subjects; the time to peak concentration was similar among the three groups. The peak plasma nilvadipine concentration was closely correlated both with the serum albumin level and the retention of indocyanine green. Changes in blood pressure, pulse rate and various vasoactive hormones following a single oral dose of nilvadipine did not differ between the groups. Thus, an increase in plasma nilvadipine relative to the level in normal subjects was demonstrated in patients with cirrhosis following a single oral dose, as well as in patients with slight liver dysfunction following long-term oral administration.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Key words Protamine ; Blood-brain barrier ; Endogenous albumin ; Immunocytochemistry ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cellular mechanisms of blood-brain barrier (BBB) opening to endogenous albumin in the mouse brain after intracarotid infusion of solutions of protamine free base (PB) or protamine sulfate (PS) were studied using quantitative immunocytochemistry. Ultrathin sections of brain samples embedded at low temperature in Lowicryl K4M were exposed to anti-mouse albumin antiserum followed by protein A-gold. Using morphometry, the density of immunosignals (gold particles per μm2) was recorded over four compartments: vascular lumen, endothelial profiles, subendothelial space (including the basement membrane), and brain parenchyma (neuropil). In addition, the adsorption of endogenous albumin evidenced by the number of gold particles per μm of the endothelial luminal plasmalemma was quantitatively evaluated. In the applied experimental conditions, PB was found to be strongly cytotoxic as indicated by the appearance of rapid degenerative changes and the disruption of the endothelial lining with concomitant clumping of the blood plasma. The action of PS was milder, offering a better opportunity for detailed ultrastructural and morphometric examination of brain samples during consecutive steps of PS action (2, 5, 10 and 30 min). As early as 10 min after infusion of PS solution, the adsorption of blood plasma albumin to the endothelial luminal surface was increased 2.5 times. Simultaneously, the immunolabelling of the endothelial profiles and subendothelial space was significantly increased. These results suggest that BBB disruption occurs through enhanced adsorption of albumin or albumin-protamine complexes to the luminal plasmalemma, followed by transendothelial vesicular transport, rather than through modification of interendothelial junctional complexes. This process appears to be focally disseminated throughout the cerebral vascular network and declines at 30 min following infusion of PS solution.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0533
    Keywords: Protamine ; Blood-brain barrier ; Endogenous albumin ; Immunocytochemistry ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cellular mechanisms of blood-brain barrier (BBB) opening to endogenous albumin in the mouse brain after intracarotid infusion of solutions of protamine free base (PB) or protamine sulfate (PS) were studied using quantitative immunocytochemistry. Ultrathin sections of brain samples embedded at low temperature in Lowicryl. K4M were exposed to anti-mouse albumin antiserum followed by protein A-gold. Using morphometry, the density of immunosignals (gold particles per μm2) was recorded over four compartments: vascular lumen, endothelial profiles, subendothelial space (including the basement membrane), and brain parenchyma (neuropil). In addition, the adsorption of endogenous albumin evidenced by the number of gold particles per μm of the endothelial luminal plasmalemma was quantitatively evaluated. In the applied experimental conditions, PB was found to be strongly cytotoxic as indicated by the appearance of rapid degenerative changes and the disruption of the endothelial lining with concomitant clumping of the blood plasma. The action of PS was milder, offering a better opportunity for detailed ultrastructural and morphometric examination of brain samples during consecutive steps of PS action (2, 5, 10 and 30 min). As early as 10 min after infusion of PS solution, the adsorption of blood plasma albumin to the endothelial luminal surface was increased 2.5 times. Simultaneously, the immunolabelling of the endothelial profiles and subendothelial space was significantly increased. These results suggest that BBB disruption occurs through enhanced adsorption of albumin or albumin-protamine complexes to the luminal plasmalemma, followed by transendothelial vesicular transport, rather than through modification of interendothelial junctional complexes. This process appears to be focally disseminated throughout the cerebral vascular network and declines at 30 min following infusion of PS solution.
    Type of Medium: Electronic Resource
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